Oxidative stress to DNA increases with age,
study finds

Dr. Arlan Richardson (right) hoods
Michelle Hamilton during a
graduation ceremony for students in
the Graduate School of Biomedical
Sciences. She earned a Ph.D. in
physiology. Hamilton's dissertation
suggests that oxidative stress to DNA
increases with age.

The older a rodent is, the
greater the chance that its
genes have been
damaged by oxidation.
That's the conclusion of a
study conducted at the
Health Science Center
and published in the Aug.
21 issue of the
Proceedings of the
National Academy of
Sciences-USA.

The researchers
compared levels of a key
stress marker,
8-oxo-2-deoxyguanosine
(oxo8dG), in rats and
mice of various ages. The
scientists scanned liver,
kidney, brain, heart and
muscle tissue, finding that
the older the rat or
mouse, the higher the
level of the marker.
Oxo8dG is described as a
modification of a genetic
sequence.

One theory of aging is
that oxidants are
generated during normal
metabolism and can react
with DNA, the genetic
code, causing damage.
The body continuously
repairs its own DNA, but any
oxidative lesion that is
not repaired can lead
to mutations,
increasing the risk of
cancer.

This study suggests
that the age-related
increase in oxidative
lesions
in DNA could be an
important factor in the
age-related increase in
most cancers. Age is
well documented to
be the leading risk
factor for
most cancers.

The study was part of
a Ph.D. dissertation
written by Michelle
Hamilton, a former
graduate student in the
department of
physiology, with
assistance from faculty
including her mentor,
Dr. Arlan G.
Richardson, professor
of physiology, director
of the Aging Research
and Education Center,
and senior career
research scientist with
the South Texas
Veterans Health Care
System, Audie
Murphy Division.